Cancer cells need sugar to survive. Sure, there may be a few types that minimize the use of sugar. But most cancers we know of including breast, ovarian, colon, pancreas, lung, cervix, brain tumors, kidney, and many more all have one thing in common. They love sugar, better known in the body as glucose. In fact, without glucose, these cancer cells stand little chance to survive and replicate. It’s the primary reasons that cutting edge cancer research is focusing on ways to disrupt the glucose metabolism of cancer cells to find more effective, and less invasive, ways to cure cancer. This type of cancer research focuses on forcing malignant cells into starvation and self-destruction while leaving all other cells of the body healthy and unharmed.1,2
PET/CT Scans Use Glucose to Detect Cancer
If you, or a loved one has ever been diagnosed with cancer then you’ve probably gone through a PET or PET-CT scan. After my hysterectomy to remove a stage 1b cervix tumor, I had several follow-up PET-CT scans myself. Ever wonder what exactly is in that radioactive stuff they inject into your IV? The answer is simple. It’s sugar marked with a radioactive isotope. The radioactive component makes it highly visible in the scan.
If after your cancer treatment there are active malignant tumors, those tumor cells will gobble up that glucose at a very high rate. In fact, the rate at which cancer cells eat up sugar compared with healthy human cells can be up to 30 times faster! This metabolic activity “lights up” on the PET scan in any tissues where there is an active tumor. This allows medical professionals to detect remaining cancer cells that are not visible through other tests such as ultrasound or MRI.
Some studies indicate that these scans can also detect the intensity of the cancer cells, the grade of tumor, and chances of metastasis in certain types of cancer.3 The greater the intensity in some cancer types, the higher grade the tumor, and the more likely the cancer will spread throughout the body.3 However, post treatment, these tests are used to simply detect any remaining tumor activity, no matter how intense, in order to plan the next step in treatment.
Understanding Energy Metabolism
There is still a lot to learn about the metabolism of cancer cells. However, when it comes to glucose, these cells use lots of it and even become dependent on it in order to survive and multiply.2
To simplify why cancer cells need lots of glucose, let’s look at the two major energy pathways in your cells. These pathways are known as the glycolitic pathway (glycolysis) and the citric acid cycle (CAC). The CAC is also called the Krebs Cycle or Carboxylic Acid Cycle, but all three are the exact same pathway just going by a different name. These two major energy pathways, glycolysis and the CAC produce the energy for your cells and therefore the energy for your entire body. This energy is known as ATP.
Glycolysis produces very little ATP. One glucose molecule ends up producing a mere 2 ATP molecules. The CAC is much more efficient and uses something known as acetyl coenzyme A (acetyl CoA) to produce energy. In normal cells, glycolysis feeds the CAC what it needs to produce the bulk of the body’s energy. When a glucose molecule is metabolized by glycolysis (the glycolytic pathway), pyruvate is formed in addition to the two ATP molecules. This pyruvate can be converted into acetyl CoA for the CAC and lead to more than 20 molecules of ATP!
Why Cancer Cells Need Lots of Glucose
There’s one more thing to understand before seeing why cancer cells love sugar. The CAC uses oxygen to from energy, but glycolysis does not require oxygen to form energy and pyruvate. In fact, as we go about our normal tasks every day our body primarily uses the CAC for energy production, which is one reason why we need oxygen to survive. There is always some glycolysis going on, especially in the brain where glucose is absolutely essential for normal function.
Usually the only time glycolysis kicks in full force, however, is during exercise or other strenuous activities that increase oxygen use so that we can maintain a proper supply of energy without running out of oxygen. During these times glycolysis helps the body increase energy production by burning our sugar stores and feeding the CAC lots of pyruvate. As long as enough oxygen is present, however, our cells basically rely on the CAC for energy.
Cancer cells are different. Although cancer cells also use both energy pathways, glycolysis is constantly in full force within these cells. Glycolysis in cancer cells leads to more lactate production than pyruvate and they exhibit greater numbers of glucose receptors on their cell membranes. This dependence on the glycolytic pathway makes glucose seemingly necessary to keep them alive. In fact, theoretically, if we could shut down the glycolytic pathway in only cancer cells within the body, the cancer could potentially die while leaving all normal cells healthy. Unfortunately, this is no easy task. However, as previously mentioned, some cutting edge cancer research does indeed focus on the sugar metabolism of cancer cells.
Sugar Does Not Cause Cancer
While I would never recommend a cancer patient eat added sugars, it’s important to understand that this research does not mean sugar causes cancer. However, I disagree with those who suggest cancer patients should continue to eat sugar because it does not speed up the growth of tumors. While this may be true, eating processed sugars is not healthy for anybody, let alone someone with cancer.
Excessive added sugar disrupts all kinds of metabolic function, increases inflammation, disrupts hormone functions, and promotes unhealthy weight gain. While sugar may not directly cause cancer, diets high in sugar are known to increase the risk of developing certain cancers such as pancreas and colon.4,5 Furthermore, overweight and obese individuals also have higher risks for cancer and high sugar diets certainly promote weight gain.
Finally, while we do not yet have evidence to show that eating sugar speeds up the growth of cancer tumors, this doesn’t mean that restricting carbohydrate intake can’t potentially slow down the growth of cancer. In fact, current nutrition research in the cancer field is focusing on doing just that.1,2
One thing to keep in mind is that simply lowering sugar in a person’s diet does not cure cancer. The reason is because the body requires a certain amount of glucose for proper function and even in ketosis the body makes sugar. Nutrition research using the strategy of starving cancer cells combines a low carbohydrate diet with other things. Even low-dose chemotherapy is used with this strategy.
While results of human trials have yet to be published, one of the leading researchers in this area, Dr. Thomas Seyfried, claims these nutrition therapies have produced remarkable results even in stage 4 brain tumors. Unfortunately, with no published results, there is no saying whether starving cancer cells in humans is truly possible. It will likely be years before we really know.
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References:
- Zhou W, Mukherjee P, Kiebish MA, Markis WT, Mantis JG, and Seyfried TN. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Nutrition & Metabolism. 2007; 4:5 doi:10.1186/1743-7075-4-5 (https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/1743-7075-4-5#Sec20)
- Hamanaka RB and Chandel NS. Targeting glucose metabolism for cancer therapy. The Journal of Experimental Medicine. 2012; 209(2): 211-215. (http://jem.rupress.org/content/209/2/211.short)
- Macheda ML, Rogers S, and Best JD. Molecular and cellular regulation of glucosetransporter (glut) proteins in cancer. Journal of Cellular Physiology. 2005; 202: 654-662. (https://onlinelibrary.wiley.com/doi/full/10.1002/jcp.20166)
- Larsson SC, Bergkvist L, Wolk A. Consumption of sugar and sugar-sweetened foods and the risk of pancreatic cancer in a prospective study. The American Journal of Clinical Nutrition. 2006; 85(5): 1171-1176. (https://academic.oup.com/ajcn/article/84/5/1171/4649305).
- Giovannucci E. Insulin, Insulin-Like Growth Factors and Colon Cancer: A Review of the Evidence. The Journal of Nutrition. 2001; 131(11): 3109S–3120S. (https://academic.oup.com/jn/article/131/11/3109S/4686730)
